Gastão L. Soares-Filho

Panic disorder and social anxiety disorder subtypes in a caffeine challenge test

Studies have demonstrated the vulnerability of anxiety disorder patients to challenge tests. Our aim was to observe if panic disorder (PD) patients and generalized social anxiety disorder (GSAD) and performance social anxiety disorder (PSAD) patients respond in a similar way to the induction of anxiety symptoms and panic attacks by an oral caffeine challenge test. We compared 28 PD patients, 25 GSAD patients, 19 PSAD, and 26 control subjects after a 480-mg caffeine test. The patients had not received psychotropic drugs for at least a 4-week period. In a randomized double-blind experiment performed in two occasions 7 days apart, 480 mg of caffeine and a caffeine-free solution were administered and anxiety scales were administered before and after each test. A panic attack was induced in 17 (60.7%) PD patients, 4 (16.0%) GSAD patients, and 10 (52.6%) PSAD patients, during the caffeine test. None of the control subjects had a panic attack after the caffeine intake. Neither patients nor any control subject had a panic attack after drinking the caffeine-free solution. Our data suggest that there is an association between PD and PSAD hyperreactivity to an oral caffeine challenge test. The PD and PSAD patients had a higher number of induced panic attacks, some specific anxiety symptoms, and a more severe anxiety response than GSAD patients and normal volunteers.

Use of the Hospital Anxiety and Depression Scale (HADS) in a Cardiac Emergency Room – Chest Pain Unit

OBJECTIVE To determine the prevalence of anxiety and depression in patients complaining of chest pain who seek a chest pain unit attendance. INTRODUCTION Patients arriving at a Chest Pain Unit may present psychiatric disorders not identified, isolated or co-morbid to the main illness, which may interfere in the patient prognosis. METHODOLOGY Patients were assessed by the “Hospital Anxiety and Depression Scale” as a screening instrument wile following a systematized protocol to rule out the diagnosis of acute coronary syndrome and other potentially fatal diseases. Patients with 8 or more points in the scale were considered “probable case” of anxiety or depression. RESULTS According to the protocol, 59 (45.4%) of 130 patients studied presented Chest Pain of Determined Cause, and 71 (54.6%) presented Chest Pain of Indefinite Cause. In the former group, in which 43 (33.1%) had acute coronary syndrome, 33.9% were probable anxiety cases and 30.5% depression cases. In the second group, formed by patients without acute coronary syndrome or any clinical conditions involving greater morbidity and mortality risk, 53.5% were probable anxiety cases and 25.4% depression. CONCLUSION The high anxiety and depression prevalence observed may indicate the need for early and specialized approach to these disorders. When coronary arterial disease is present, this may decrease complications and shorten hospital stay. When psychiatric disorder appears isolated, is possible to reduce unnecessary repeated visits to emergency room and increase patient’s quality of life.

A randomized, naturalistic, parallel-group study for the long-term treatment of panic disorder with clonazepam or paroxetine.

Abstract This long-term extension of an 8-week randomized, naturalistic study in patients with panic disorder with or without agoraphobia compared the efficacy and safety of clonazepam (n = 47) and paroxetine (n = 37) over a 3-year total treatment duration. Target doses for all patients were 2 mg/d clonazepam and 40 mg/d paroxetine (both taken at bedtime). This study reports data from the long-term period (34 months), following the initial 8-week treatment phase. Thus, total treatment duration was 36 months. Patients with a good primary outcome during acute treatment continued monotherapy with clonazepam or paroxetine, but patients with partial primary treatment success were switched to the combination therapy. At initiation of the long-term study, the mean doses of clonazepam and paroxetine were 1.9 (SD, 0.30) and 38.4 (SD, 3.74) mg/d, respectively. These doses were maintained until month 36 (clonazepam 1.9 [SD, 0.29] mg/d and paroxetine 38.2 [SD, 3.87] mg/d). Long-term treatment with clonazepam led to a small but significantly better Clinical Global Impression (CGI)–Improvement rating than treatment with paroxetine (mean difference: CGI-Severity scale −3.48 vs −3.24, respectively, P = 0.02; CGI-Improvement scale 1.06 vs 1.11, respectively, P = 0.04). Both treatments similarly reduced the number of panic attacks and severity of anxiety. Patients treated with clonazepam had significantly fewer adverse events than those treated with paroxetine (28.9% vs 70.6%, P < 0.001). The efficacy of clonazepam and paroxetine for the treatment of panic disorder was maintained over the long-term course. There was a significant advantage with clonazepam over paroxetine with respect to the frequency and nature of adverse events.

Tapering clonazepam in patients with panic disorder after at least 3 years of treatment.

High-potency benzodiazepines, such as clonazepam, are frequently used in the treatment of panic disorder (PD) because of their rapid onset of action and good tolerability. However, there is concern about their potential to cause withdrawal symptoms. We aimed to develop a protocol for safely tapering off clonazepam in patients with PD who had been receiving treatment for at least 3 years. A specific scale for judging withdrawal was also developed, the Composite Benzodiazepine Discontinuation Symptom Scale. We selected 73 patients with PD who had been asymptomatic for at least 1 year and who wished to discontinue the medication. The trial consisted of a 4-month period of tapering and an 8-month follow-up period. The dosage of clonazepam was decreased by 0.5 mg per 2-week period until 1 mg per day was reached, followed by a decrease of 0.25 mg per week. The mean dosage at the start of tapering was 2.7 ± 1.2 mg/d. In total, 51 (68.9%) of the patients were free of the medication after the 4 months of tapering according to the protocol, and 19 (26.0%) of the patients needed another 3 months to be free of medication. Clonazepam discontinuation symptoms were mostly mild and included mainly: anxiety, shaking/trembling/tremor, nausea/vomiting, insomnia/nightmares, excessive sweating, tachycardia/palpitations, headache, weakness, and muscle aches. The improvement in PD and general well-being was maintained during both the taper and follow-up phases. Clonazepam can be successfully discontinued without any major withdrawal symptoms if the dose is reduced gradually. We recommend reducing the dosage of clonazepam after intermediate-term use by 0.25 mg/wk.

Double-blind comparison of 30 and 60 mg tranylcypromine daily in patients with panic disorder comorbid with social anxiety disorder

Our objective was to explore the dose-response relationship in patients with panic disorder and social anxiety disorder comorbidity (DSM-IV). After 1 week of no-drug washout, 36 such patients were assigned to a double-blind controlled comparison of the effects of 30 mg and 60 mg of tranylcypromine, and were followed up for 12 weeks. The main instrument used to measure the number of panic attacks was the Sheehan Panic and Anticipatory Anxiety Scale. The primary outcome measure for social anxiety disorder symptoms was the mean change from baseline in the Liebowitz Social Anxiety Scale (LSAS). After 12 weeks of treatment, panic attacks were reduced 69.6% from baseline in the 30-mg group (n=19) compared with a 74.8% reduction in the 60-mg group (n=17). Twelve patients (70.6%) of the higher dose group and 14 patients (68.4%) of the lower dose were completely free of panic attacks. There was no difference in efficacy between the tranylcypromine groups in the panic disorder symptoms. The 60-mg dose was more efficacious as measured by the LSAS scores, showing a significant difference in relation to the lower group. Mean change from baseline in LSAS total score (mean+/-SD) for 30-mg group was 17.9+/-14.7 and for the 60-mg group was 35.0+/-14.8. The social anxiety symptom scale showed a two-fold greater change with the 60-mg dose, and the 30-mg dose group could be considered the equivalent of a placebo control group. Tranylcypromine--60 mg daily--was found effective in the treatment of panic disorder and social anxiety disorder comorbidity.

Chest pain, panic disorder and coronary artery disease: a systematic review.

Chest pain may be due benign diseases but often suggests an association with coronary artery disease, which justifies a quick search for medical care. However, some people have anxiety disorder with symptoms that resemble clearly an acute coronary syndrome. More specifically, during a panic attack an abrupt feeling of fear accompanied by symptoms such as breathlessness, palpitations and chest pain, makes patients believe they have a heart attack and confuse physicians about the diagnosis. The association between panic disorder and coronary artery disease has been extensively studied in recent years and, although some studies have shown anxiety disorders coexisting or increasing the risk of heart disease, one causal hypothesis is still missing. The aim of this systematic review is to present the various ways in which the scientific community has been investigating the relation between chest pain, panic disorder and coronary artery disease.

Efficacy of cognitive behavioral therapy in reducing psychiatric symptoms in patients with implantable cardioverter defibrillator: an integrative review.

This article is a systematic review of the available literature on the benefits that cognitive behavioral therapy (CBT) offers patients with implanted cardioverter defibrillators (ICDs) and confirms its effectiveness. After receiving the device, some patients fear that it will malfunction, or they remain in a constant state of tension due to sudden electrical discharges and develop symptoms of anxiety and depression. A search with the key words “anxiety”, “depression”, “implantable cardioverter”, “cognitive behavioral therapy” and “psychotherapy” was carried out. The search was conducted in early January 2013. Sources for the search were ISI Web of Knowledge, PubMed, and PsycINFO. A total of 224 articles were retrieved: 155 from PubMed, 69 from ISI Web of Knowledge. Of these, 16 were written in a foreign language and 47 were duplicates, leaving 161 references for analysis of the abstracts. A total of 19 articles were eliminated after analysis of the abstracts, 13 were eliminated after full-text reading, and 11 articles were selected for the review. The collection of articles for literature review covered studies conducted over a period of 13 years (1998-2011), and, according to methodological design, there were 1 cross-sectional study, 1 prospective observational study, 2 clinical trials, 4 case-control studies, and 3 case studies. The criterion used for selection of the 11 articles was the effectiveness of the intervention of CBT to decrease anxiety and depression in patients with ICD, expressed as a ratio. The research indicated that CBT has been effective in the treatment of ICD patients with depressive and anxiety symptoms. Research also showed that young women represented a risk group, for which further study is needed. Because the number of references on this theme was small, further studies should be carried out.

Myocardial Perfusion Imaging Study of CO2-Induced Panic Attack

Chest pain is often seen alongside with panic attacks. Moreover, panic disorder has been suggested as a risk factor for cardiovascular disease and even a trigger for acute coronary syndrome. Patients with coronary artery disease may have myocardial ischemia in response to mental stress, in which panic attack is a strong component, by an increase in coronary vasomotor tone or sympathetic hyperactivity setting off an increase in myocardial oxygen consumption. Indeed, coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. These findings correlating panic disorder with coronary artery disease lead us to raise questions about the favorable prognosis of chest pain in panic attack. To investigate whether myocardial ischemia is the genesis of chest pain in panic attacks, we developed a myocardial perfusion study through research by myocardial scintigraphy in patients with panic attacks induced in the laboratory by inhalation of 35% carbon dioxide. In conclusion, from the data obtained, some hypotheses are discussed from the viewpoint of endothelial dysfunction and microvascular disease present in mental stress response.

Psychiatric Disorders and Quality of Life in Patients With Implantable Cardioverter Defibrillators: A Systematic Review

OBJECTIVE To systematically review the literature with regard to psychiatric disorders and quality of life in patients with an implantable cardioverter defibrillator. DATA SOURCES Research was conducted in 3 databases (ISI Web of Science, PubMed, and PsycINFO) using the terms implantable, cardioverter, defibrillator, quality of life, psych *, anxiety, and depression. STUDY SELECTION The search yielded 1,399 references. Non-English and repeated references were excluded. After abstract analysis, 42 references were recovered for full-text reading, and 25 articles were selected for this review. DATA EXTRACTION Research took place in April 2012, and no time restriction was placed on any of the database searches. Review or theoretical articles were excluded, and only clinical trials and epidemiologic studies were selected for this review. RESULTS A systematic review of the literature revealed mostly observational prospective cohort studies followed by cross-sectional observational studies and randomized clinical trials. Few studies included in the review were observational retrospective cohort or case-control studies. There are prominent signs and symptoms of anxiety and depression in patients with an implantable cardioverter defibrillator. Disorders include phobic anxiety, posttraumatic stress disorder, panic disorder, somatoform disorder, agoraphobia, and depression. Quality of life in the physical, social, and psychological domains is affected and is related to the intensity and the frequency of the devices electrical discharge. CONCLUSIONS Work regarding psychiatric comorbidity in patients with an implantable cardioverter defibrillator has shown that anxiety and depression are common. The patients and their families should be informed by their doctors that the presence of the device minimizes risk of sudden death and allows them to have a normal life.

Panic attack triggering myocardial ischemia documented by myocardial perfusion imaging study. A case report

Background Chest pain, a key element in the investigation of coronary artery disease is often regarded as a benign prognosis when present in panic attacks. However, panic disorder has been suggested as an independent risk factor for long-term prognosis of cardiovascular diseases and a trigger of acute myocardial infarction. Objective Faced with the extreme importance in differentiate from ischemic to non-ischemic chest pain, we report a case of panic attack induced by inhalation of 35% carbon dioxide triggering myocardial ischemia, documented by myocardial perfusion imaging study. Discussion Panic attack is undoubtedly a strong component of mental stress. Patients with coronary artery disease may present myocardial ischemia in mental stress response by two ways: an increase in coronary vasomotor tone or a sympathetic hyperactivity leading to a rise in myocardial oxygen consumption. Coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. Possibly the carbon dioxide challenge test could trigger myocardial ischemia by the same mechanisms. Conclusion The use of mental stress has been suggested as an alternative method for myocardial ischemia investigation. Based on translational medicine objectives the use of CO2 challenge followed by Sestamibi SPECT could be a useful method to allow improved application of research-based knowledge to the medical field, specifically at the interface of PD and cardiovascular disease.